Before performing these experiments, Lewis' team first looked at signals of a fluorescent dye, which previous researchers had used as an indicator for ROS levels. The team treated bacterial cells with a variety of antibiotics and measured the strength of this signal. Since antibiotics were presumed to increase ROS levels, one would have expected increased concentrations of antibiotics to correlate with stronger signals. However, Lewis' group saw no such correlation.
"But there's a difference between correlation and direct observation," Keren said. In order to support their observations with unequivocal data, the team members physically separated the cells that had stronger fluorescent signals from those with weak signals and treated them both with the same antibiotics. Both populations suffered equivalent cell death.
"The research from Dr. Lewis' group demonstrates that, contrary to current dogma, antibiotics apparently do not kill bacteria through induction of reactive oxygen species," said Steven Projan, vice president for research and development at iMed and head of Infectious Diseases and Vaccines at MedImmune, both subsidiaries of AstraZeneca. "The results shown are rather clear but still leave us with the mystery as to how antibacterial drugs help infected people clear bacterial infections. At this point, we should probably dispense with the 'one size fits all' approach to bacterial killing by antibiotics," said Projan, who was not involved in the research.
With these results, Lewis and Keren hope the field will be able to focus its efforts on understanding the true mechanisms of how antibiotics wipe out bacteria in order to effectively address chronic bacterial infections, one of the most pressing issues facing public health today.
|Contact: Lori Lennon|
Northeastern University College of Science